Ecologists use oceanographic data to predict future climate change

Past ocean circulation leads to new conclusions
Ecologists and oceanographers are attempting to predict the future impacts of climate change by reconstructing the past behavior of Arctic climate and ocean circulation.
In a November special issue of the journal Ecology, a group of scientists report that if current patterns of change in the Arctic and North Atlantic Oceans continue, alterations of ocean circulation could occur on a global scale, with potentially dramatic implications for the world’s climate and biosphere.

“This research presents a compelling example of how climate change has altered marine ecosystems,” said David Garrison, director of the National Science Foundation (NSF)’s Biological Oceanography Program, which funded the research. “It illustrates the value of basic research in understanding the underlying mechanisms and consequences of rapid climate change.”

Charles Greene of Cornell University and colleagues reconstructed the patterns of climate change in the Arctic from the Paleocene epoch to the present.

Over these 65 million years, the Earth has undergone several major warming and cooling episodes, which were largely mitigated by the expansion and contraction of sea ice in the Arctic.

“When the Arctic cools and ice sheets and sea ice expand, the increased ice cover increases albedo, or reflectance of the sun’s rays by the ice,” says Greene, the lead author on the paper. “When more of the sun is reflected rather than absorbed, this leads to global cooling.”
Likewise, when ice sheets and sea ice contract and expose the darker-colored land or ocean underneath, heat is absorbed, accelerating climate warming.

Currently, the Earth is in the midst of an interglacial period, characterized by retracted ice sheets and warmer temperatures.

In the past three decades, changes in Arctic climate and ice cover have led to several reorganizations of northern ocean circulation patterns.

Since 1989, a species of plankton native to the Pacific Ocean has been colonizing the North Atlantic Ocean, a feat that hasn’t occurred in more than 800 thousand years. These plankton were carried across the Arctic Ocean by Pacific waters that made their way to the North Atlantic.

“When Arctic climate changes, waters in the Arctic can go from storing large quantities of freshwater to exporting that freshwater to the North Atlantic in large pulses, referred to as great salinity anomalies,” Greene explains. “These GSAs flow southward, disrupting the ocean’s circulation patterns and altering the temperature stratification observed in marine ecosystems.”

In the continental shelf waters of the Northwest Atlantic, the arrival of a GSA during the early 1990s led to a major ecosystem reorganization, or regime shift. Some ocean ecosystems in the Northwest Atlantic saw major drops in salinity, increased stratification, an explosion of some marine invertebrate populations and a collapse of cod stocks.

“The changes in shelf ecosystems between the 1980s and 1990s were remarkable,” says Greene. “Now we have a much better idea about the role climate had in this regime shift.”
The changes observed in recent decades are only the tip of the iceberg. Previous interglacial periods have ended when the global ocean’s deep circulation slowed in response to reductions in the formation of North Atlantic Deep Water, or NADW, a large, deep mass of highly saline water in the North Atlantic.
At these tipping points in the Earth’s history, NADW formation was disrupted by pulses of freshwater entering the North Atlantic. The slowing of the global ocean’s deep circulation results in less heat being transported to higher latitudes, accelerating ice formation and advancing the Earth into glacial conditions.

Recent modeling studies show that NADW formation will likely be resilient to freshwater pulses from the Arctic during the 21st century, according to the authors.
Continued exposure to such freshwater forcing, however, could disrupt global ocean circulation during the next century and lead to very abrupt changes in climate, similar to those that occurred at the onset of the last ice age.

“If the Earth’s deep ocean circulation were to be shut down, many of the atmospheric, glacial and oceanic processes that have been stable in recent times would change, and the change would likely be abrupt,” says Greene.

“While the ecosystem consequences of gradual changes in the ocean are somewhat predictable, all bets are off after such abrupt changes
He points out that calcitriol is involved in cell cycle regulation and control of proliferation, cellular differentiation and communication between cells, as well as programmed cell death (apoptosis and autophagy) and antiangiogenesis.

Calcitriol is the form of vitamin D that activates the body’s Vitamin D Receptor (VDR), which allows gene transcription to take place and the activation of the innate immune response.

It is possible that several of the transcribed by the VDR will help transcribe proteins that protect the body against radiation.

“Vitamin D by its preventive/ameliorating actions should be given serious consideration as a protective agent against sublethal radiation injury, and in particular that induced by low-level radiation,” concludes Hayes.

Could vitamin D save us from radiation?

Radiological health expert Daniel Hayes, Ph.D., of the New York City Department of Health and Mental Hygiene suggests that a form of vitamin D could be one of our body’s main protections against damage from low levels of radiation.

Writing in the International Journal of Low Radiation, Hayes explains that calcitriol, the active form of vitamin D, may protect us from background radiation and could be used as a safe protective agent before or after a low-level nuclear incident.

Biologists and pharmacologists who specialize in radiation and health are keen to find an effective agent that could be given by mouth, have few side effects and would protect us against a suspected or impending nuclear event, whether an accident, terrorist attack, or other incident.

In terms of protecting people from the long-term effects of radiation, cancer formation would be the main focus. The ideal agent would act by blocking DNA damage or by halting the progression of damaged cells that might eventually grow into cancers.

While a drug is yet to be found with such ideal radio-protective properties, other researchers have demonstrated that certain dietary supplements have at least some of the desired properties. Hayes argues that vitamin D, and in particular its biologically active form,
could be the key ingredient in radiological protection.

“Our general understanding and appreciation of the multifaceted protective actions of vitamin D have recently entered a new era,” says Hayes, “It is now becoming recognized that its most active molecular form, 1,25-dihydroxyvitamin D3,
may offer protection against a variety of radiation- and otherwise-induced damages.”
Hayes has reviewed the various biochemical mechanisms by which vitamin D protects users_ from the low levels of natural radiation released by the rocks on which we stand and the skies above us.

Even plants benefit from outsourcing

The answer to successful revegetation of native flora is in sourcing genetically diverse seed not necessarily relying on remnant local native vegetation to provide seed.

“A common belief is that local native plants are the best source of seed for revegetation projects,” says Dr Linda Broadhurst from CSIRO, Australia’s national science agency.

“It has been presumed that local seed is adapted to local conditions and therefore it would provide the best results for restoration projects.”

“However, the research shows that where vegetation loss is high and across large areas, ‘local’ seed sources are often small and isolated and can be severely inbred resulting in poor seed crops or low quality seed.”

“This can lead to germination failure and poor seedling growth.”

Land and water degradation resulting from vegetation clearance is a global problem. Effective restoration techniques are essential in reducing the damage and improving the environment.

In an effort to help, Dr Broadhurst and her colleagues have published a review on the issues associated with collecting seed for broadscale restoration projects in the new journal Evolutionary Applications (Volume 1, Issue 4).

The review covers the appropriateness of using ‘local’ seed, how much seed and the types of populations that should be sampled, and the impact that over-harvesting might have on remnant populations.

“The current emphasis on using local seed sources for revegetation will, in many cases, lead to poor restoration outcomes,” says Dr Broadhurst.

“Our findings show that seed sourcing should concentrate less on collecting from local environments and more on capturing high quality and genetically diverse seed.”

“This will ensure that restored populations have ample genetic diversity to respond to changing environments over the coming decades.”

Scientists identify machinery that helps make memories

DURHAM, N.C. — A major puzzle for neurobiologists is how the brain can modify one microscopic connection, or synapse, at a time in a brain cell and not affect the thousands of other connections nearby. Plasticity, the ability of the brain to precisely rearrange the connections between its nerve cells, is the framework for learning and forming memories.

Duke University Medical Center researchers have identified a missing-link molecule that helps to explain the process of plasticity and could lead to targeted therapies.

The discovery of a molecule that moves new receptors to the synapse so that the neuron (nerve cell) can respond more strongly helps to explain several observations about plasticity, said Michael Ehlers, M.D., Ph.D., a Duke professor of neurobiology and senior author of the study published in the Oct. 31 issue of Cell.

“This may be a general delivery system in the brain and in other types of cells, and could have significance for all cell signaling.”

Ehlers said this could be a general way for all cells to locally modify their membranes with receptors, a process critical for many activities — cell signaling, tumor formation and tissue development.

“Part of plasticity involves getting receptors to the synaptic connections of nerve cells,” Ehlers said. “The movement of neurotransmitter (chemical) receptors occurs through little packages that deliver molecules to the synapse when new memories form.What we have discovered is the molecular motor that moves these packages when synapses are active.”

When neurons fire at the same time, their connections strengthen and a person can associate certain features. “Once you have heard someone’s name, seen his face, where he was standing,
all these features can be bound into a unified packet of information – a percept – and at a very cellular level this occurs
by strengthening synaptic connections between co-active neurons,” said Ehlers, who is also a Howard Hughes Medical Investigator.

To learn and make new associations, the brain alters the strengths of the synapses’ electrical inputs onto cells that compute these features. Scientists studied the hippocampus,
where memories form, but this machinery could operate in other brain areas.“One of earliest changes in Alzheimer’s disease is synapse dysfunction, so this molecule might be a new target for that disease,” he said.

“Abnormal movement of receptors may be implicated in brain development, in autism.” He said the molecule potentially is involved “in the abnormal electrical activity of epilepsy and the overactive brain pathways of addiction.”

In a series of biochemistry and microscopic imaging experiments, Ehlers and colleagues found that the myosin Vb (five-b) molecule in hippocampal neurons responded to a flow of calcium ions from the synaptic space by popping up and into action.

One end of the myosin is attached the meshlike actin filaments so it can “walk” to the end of the nerve cells where receptors are. On its other end, it tows an endosome, a packet that contains new receptors.

“These endosomes are like little memories waiting to happen,” Ehlers said. “They are reservoirs of neurotransmitter receptors that brain cells deploy to add more receptors to a particular synapse. More receptors equals stronger synapses.”

Electrical impulses cause one nerve cell to dump its neurotransmitter, in this case, glutamate, into the small space between neurons (the synapse), which activates neurotransmitter receptors on the receiving side. These are ion channels that open in response to neurotransmitter and generate the electrical impulse.

When the scientists blocked myosin in single cells, this stopped the addition of new receptors and prevented electrical impulses from getting stronger, showing that myosin is essential to enhancing nerve cell connections.

“This is a very basic cellular mechanism of brain plasticity. It is likely fundamental to brain development and disease,” Ehlers said. “The myosin Vb molecule gives us a new way to think about designing therapies for treating memory loss, psychiatric disease and brain development.”

Crucial hormonal pathway to bone building uncovered

Study authors find a novel mechanism for how parathyroid hormone signaling selectively stimulates bone formation

BIRMINGHAM, Ala. – Scientists have discovered a crucial step in hormone-triggered bone growth,
a finding that could lead to new osteoporosis drugs and better bone-building therapies, according to a new study.

The research was performed at the University of Alabama at Birmingham (UAB). It showed
that parathyroid hormone (PTH) given intermittently enhances the body’s own bone-building action
through a specific “co-receptor” on the surface of bone cells.

Previously, PTH was known to stimulate bone formation, but the exact mechanism was unknown, the UAB researchers said.

The findings are published in the journal Genes and Development.

“Our study uncovers a novel mechanism for how parathyroid hormone signaling selectively stimulates bone formation,” said Xu Cao, Ph.D.,

UAB professor of pathology and senior author on the study. “We have identified the protein co-receptor crucial to the whole process.”

The UAB researchers focused on PTH signals in mice, testing to see which cell receptors actively recruited calcium from the blood.

They uncovered the one co-receptor responsible for turning on bone building, said Mei Wan, Ph.D., UAB associate professor of molecular and cellular pathology and first author on the study.

Previously, the exact mechanism of PTH-signaled bone formation was shrouded by the joint production of osteoblasts and osteoclasts,

said Jay McDonald, M.D., pathology professor and director of UAB’s Center for Metabolic Bone Disease. Both types of cells are instrumental in regulating a healthy skeleton – osteoblasts by forming new bone, and osteoclasts by resorbing old and brittle bone.

Many osteoporosis drugs now target both osteoblasts and osteoclasts, which can lead to zero or minimal bone formation, McDonald said.

“The ideal would be to have one drug to shut down the osteoclasts and turn on the osteoblasts to effectively build bone. We don’t have that yet, but this study shows us the path to get there,” he said.

FORTEO® is the only approved PTH drug for use in postmenopausal women with osteoporosis, and in men with hormone-linked osteoporosis.Many experts hope the approved drug is part of the next wave of medicines that work to build back bone, reduce bone loss and minimize fracture risks in the aging.

Simple chemical procedure augments therapeutic potential of stem cells

BOSTON, Mass. (Oct. 31, 2008) — Adult stem cells resemble couch potatoes if they hang out and divide in a dish for too long. They get fat and lose key surface proteins, which interferes with their movement and reduces their therapeutic potential. Now, via a simple chemical procedure, researchers have found a way to get these cells off the couch and over to their therapeutic target.

To do this, they simply added a molecule called SLeX to the surface of the cells. The procedure took just 45 minutes and restored an important biological function.

“Delivery remains one of the biggest hurdles to stem cell therapy,” explains senior author Jeffrey Karp, an instructor at the Harvard-MIT Division of Health Sciences and Technology.

“The blood stream offers a natural delivery vehicle, but stem cells don’t move through blood vessels normally after being expanded in culture. Our procedure promises to overcome this obstacle.”

These findings will be published online in the journal Bioconjugate Chemistry on Oct. 31.

In order for cells injected into the blood stream to be therapeutically useful, they need to take initiative to reach target tissues. But instead, cultured stem cells go with the flow.

They move through the body quickly, carried by the current, which means they seldom contact the sides of blood vessels. Thus, they have fewer opportunities to escape into the surrounding tissue by squeezing between cells of the vessel wall.

Adult stem cells must escape before they can colonize surrounding tissue and rebuild damaged structures.

In February of 2008, HMS associate professor Robert Sackstein (at Brigham and Women’s Hospital) and colleagues showed they could correct this problem by adding a particular molecule to the surface of adult stem cells.

This molecule—a cousin of SLeX—formed temporary connections with proteins on the blood vessel wall, serving as a kind of weak tape. But Sackstein’s method involved enzymes, which made the chemistry complicated. Karp’s team achieved the same result without enzymes.

Karp lab postdoc Debanjan Sarkar simply flooded a dish of cells with three molecules—biotin, streptavidin, and SLeX—one after the other. The biotin and streptavidin anchored SLeX to the cell surface.

Sarkar tweaked the concentrations of each molecule to maximize the cell’s ability to roll along the interior of the blood vessel, rather than getting lost in the flow. He also confirmed that the altered cells were still viable.

“The method is very simple,” says Sarkar, who is first author on the paper. “Plus, biotin and streptavidin work with many molecules, so labs can use this universal anchor we discovered to tackle other problems. They’re not limited to sticking SLeX on cells.”

The team worked with human cells extracted from the bone marrow. The cultures included mesenchymal stem cells (MSCs), which can form fat cells, cartilage, bone, tendon and ligaments, muscle cells, and even nerve cells.

When injected into the bloodstream of patients, MSCs can home to the site of an injury and replace damaged tissue.

But just a fraction of cultured MSCs currently reach their target in clinical trials. Karp’s procedure might improve their homing abilities.

Karp cautions that his lab’s discovery must be validated in animals, before doctors can apply it in the clinic. He’s collaborating with another lab to test the homing ability of the SLeX-dotted cells in mice.
“We need to confirm that this rolling behavior translates into increased homing and tissue repair,” explains Karp. “We may need to tweak the cells further.”

“This is definitely an approach that should be tried,” adds Pamela Robey, chief of the Craniofacial and Skeletal Diseases Branch of the National Institute of Dental and Craniofacial Research.

Robey is working to reconstruct three-dimensional tissues with MSCs. “Jeff hasn’t tested the altered MSCs inside animals, and that’s really the gold-standard, but his in vitro data looks promising

Study sheds light on genetic differences that cause a childhood eye disease

Medical researchers at the University of Alberta have unlocked part of the mystery underlying a childhood eye disease.

New research shows how children with some types of glaucoma end up with missing or extra pieces of DNA.

The missing or extra bits of DNA are called copy number variations (CNVs). The U of A research team had previously shown how they play a major role
in causing some types of pediatric glaucoma – a disease that can lead to blindness.
In their current study, published in Human Molecular Genetics, the authors describe how the CNVs that cause childhood glaucomas are formed.

Using genetic samples from patients living with pediatric glaucoma, the research team studied the locations where extra or missing pieces of DNA begin and end.

Close examination of these break points allowed the team to determine how these copy number variations occur.

The research team has received funding from the Emerging Research Teams Grant Program, which was created by the Faculty of Medicine & Dentistry and Alberta Health Services to provide startup money to promising research groups.

The study was undertaken in collaboration with researchers at the University of Chicago, the Wellcome Trust Sanger Institute, the Leicester Royal Infirmary and the UCL Institute of Child Health.

Bacteria manage perfume oil production from grass

Scientists in Italy have found bacteria in the root of a tropical grass whose oils have been used in the cosmetic and perfumery industries.

These bacteria seem to promote the production of essential oils,
but also they change the molecular structure of the oil, giving it different flavours and properties: termicidal, insecticidal, antimicrobial and antioxidant.

Studying the root of the tropical Vetiver grass through interdisciplinary research, the microbiologists Pietro Alifano and Luigi Del Giudice,
the plant biologist Massimo Maffei and their colleagues found that Vetiver root cells produce a few oil precursors, which are then metabolised by the root bacteria to build up the complexity of the Vetiver oil.

The bacteria were found in the oil-producing cells as well as in root locations that are closely associated with the essential oil.

The Vetiver grass is the only grass cultivated specifically for its root essential oil, which is made up of chemicals called sesquiterpenes.

These are used in plants as pheromones and juvenile hormones. The essential oils also contain alcohols and hydrocarbons, which, together with the sesquiterpenes are primarily used in perfumery and cosmetics.

The perfumery and flavouring industry could benefit from the increased variety that these bacteria provide to the smells and tastes of these oils
The bacteria responsible for this transformation include alpha-, beta- and gamma-proteobacteria, high-G+C Gram-positive bacteria as well as microbes which belong to the Fibrobacteres / Acidobacteria group.

“This research opens new frontiers in the biotech arena of natural bioactive compounds” said Professor Alifano “Pharmaceutical, perfumery and flavouring industries may now exploit the selected microbial strains and widen their metabolic libraries”.

“The ecological role of plant-microbial associations shows another fascinating aspect” said Professor Maffei “The metabolic interplay between a plant, which offers a few simple molecules, with root bacteria, that biotransform them into an array of bioactive compounds,
increases fitness and reveals new cost-efficient survival strategies”

Corn researchers discover novel gene shut-off mechanisms

3:34 p.m., Oct. 30, 2008—-University of Delaware scientists, in collaboration with researchers from the University of Arizona and South Dakota State University,
have identified unusual differences in the natural mechanisms that turn off, or “silence,” genes in corn.
The discovery, which was made by comparing the impact of inactivating a gene that occurs in both corn and in the much-studied laboratory plant Arabidopsis, provides new insight into how one of the world’s most important crops protects itself from mutation-causing mobile DNA elements and viruses.
The research was led by Blake Meyers, associate professor of plant and soil sciences, and Pamela Green, Crawford H. Greenewalt Chair and professor of plant and soil sciences and marine bioscience, and their laboratory groups at the Delaware Biotechnology Institute, a major center for biotechnology and life sciences research at the University of Delaware.

Collaborating with the University of Delaware team were Vicki Chandler, the Carl E. and Patricia Weiler Endowed Chair for Excellence in Agriculture and Life Sciences Regents’ Professor at the University of Arizona, and Yang Yen, a professor at South Dakota State University.

The results were published in the Proceedings of the National Academy of Sciences of the United States of America.

Studies of Arabidopsis thaliana, a small flowering plant of the mustard family that is easy to grow in the lab, have provided a lot of what scientists know about gene silencing in plants.

An important key to the process is short sequences of ribonucleic acids known as “small RNAs” which act like biochemical switches that shut off genes, thus playing a fundamental role in plant development. Understanding how small RNAs work is a continuing quest for geneticists seeking to breed plants with improved crop yields, disease resistance and other characteristics.

Previously, the Meyers and Green labs had studied Arabidopsis plants with nonfunctional versions of a gene known as RNA-dependent RNA polymerase 2 (RDR2). Without an active copy of this gene, the plants were unable to produce a major class of small RNAs, which act to stabilize and protect genes on the chromosomes.

In that prior work, Meyers and Green took advantage of the nonfunctional gene to study microRNAs, an interesting type of small RNA that is usually “masked” by the major class of small RNAs produced by RDR2.

Independently of the UD groups, Chandler and her team at the University of Arizona had identified from corn an orthologous gene–a gene that has the same function in different organisms. In corn, this gene, which the Chandler lab found, is called the mediator of paramutation (MOP1). Its equivalent in Arabidopsis is the RDR2 gene.

Because the RDR2 and MOP1 genes should both produce the “protective” set of small RNAs, the research groups decided to collaborate to see if the small RNAs in corn behave the same way they do in Arabidopsis.

The hypothesis was that the result would be the same in the two plant species, and the lab groups could use the MOP1 corn plants to focus their studies on the harder-to-examine microRNAs, as they had done previously in Arabidopsis.

“Yet we found something that had not been observed before in this plant–an odd class of small RNAs,” Meyers said. “I think it’s pretty neat to work in a more complex system like corn and see things that Arabidopsis hadn’t shown us,” he noted.

Using a technique known as sequencing by synthesis (SBS), provided by Illumina in Hayward, Calif., coupled with state-of-the-art bioinformatics in Meyers’ lab, the research team found that the MOP1 and RDR2 genes are not fully equivalent based on an assessment of small RNA complexity.

The researchers found that there are lots more RNAs of an unusual class known as “small interfering RNAs” in corn than there are in Arabidopsis.

“This class of RNAs mainly functions to repress repetitive sequences, including mobile DNA elements called transposons,” Meyers said. “Thus, small interfering RNAs act to protect the genome,” he noted.
“Corn contains an extra layer of protective small RNAs that had not been observed in Arabidopsis, so there must be additional genes other than MOP1 that produce this,” Meyers said.

The scientific community is sequencing the corn genome now, Meyers said. Once the genome is available, the work of matching up small RNAs to specific traits in corn will be much easier, he noted.

“This research is helping us to better understand the biology of corn–one of the most important plants in the world–and gives us new avenues for exploring a novel class of small RNAs,” Meyers said.